Cytokine and chemokine receptor profile of peripheral blood mononuclear cells during treatment with infliximab in patients with active rheumatoid arthritis

Abstract

Objectives: To analyse immunological changes during treatment with a monoclonal anti-tumour necrosis factor a (TNFa) antibody, infliximab, in patients with rheumatoid arthritis (RA). Methods: 25 patients with RA and 5 patients with other arthritides were studied during the first 6 weeks of treatment with infliximab. At the start of treatment and after 2 and 6 weeks, spontaneous expression of CCR3 and CCR5 on peripheral blood T cells and monocytes was studied by flow cytometry.

Anti-TNF therapy in patients with rheumatoid arthritis decreases Th1 and Th17 cell populations and expands IFN-γ-producing NK cell and regulatory T cell subsets

“…This result disagrees with several studies reporting an attenuated Th1 response in RA patients, which is restored by anti-TNF therapy, even after a single dose (Aerts et al 2010;Berg et al 2001;Kawashima and Miossec 2005;Maurice et al 1999;Nissinen et al 2004;Schuerwegh et al 2003). The discrepancies between those results and ours could reside in many factors, such as the length of the studies or the methodology applied to measure T helper responses, which in some cases is not accurate enough to discriminate between different IFN-␥-secreting cell types.…”

“…The discrepancies between those results and ours could reside in many factors, such as the length of the studies or the methodology applied to measure T helper responses, which in some cases is not accurate enough to discriminate between different IFN-␥-secreting cell types. In addition, the nature of the stimulus used differs among the studies and include microbial or self antigens (Berg et al 2001), cytokines (Kawashima and Miossec 2005) or mitogens such as phytohemagglutinin (Nissinen et al 2004) or PMA plus ionomycin (Maurice et al 1999;Schuerwegh et al 2003). Only one previous work studied Th1 cells in RA patients undergoing adalimumab therapy, reporting an increase of IFN-␥ secretion by PBMCs stimulated with anti-CD3 plus anti-CD28 antibodies (Aerts et al 2010).…”

Disease Activity and Cytokine Production in Mitogen-Stimulated Peripheral Blood Mononuclear Cells from Patients with Rheumatoid Arthritis

“…However, in our study it was noted that regardless of which medications were used to induce remission in RA patients, there were no significant differences in the cytokine levels or ratios in patients with active disease compared to those in remission. The effects of DMARD on cytokine levels in RA are not consistent, with most studies showing mixed results [33][34][35] . It has been hypothesized that DMARD may lead to restoration of peripheral cell-mediated immunity as a response to treatment [34] .…”

“…The effects of DMARD on cytokine levels in RA are not consistent, with most studies showing mixed results [33][34][35] . It has been hypothesized that DMARD may lead to restoration of peripheral cell-mediated immunity as a response to treatment [34] .…”

In Vitro Effects of Mevastatin and Biological Preparations Upon Activation of Ebv-Specific Cd4+t Lymphocytes From the Patients With Rheumatoid Arthritis

“…В ряде исследований продемонстрировано уменьшение ответа Т-лимфоцитов перифери-ческой крови больных РА на стимуляцию раз-личными антигенами или митогенами [13,17]. Аллель HLA-DRB1*0404, предрасполагающий к развитию РА, ассоциирован со снижением со-держания Т-лимфоцитов, специфичных к ан-тигену ВЭБ gp110, который является гликопро-теином репликативной фазы и играет важную роль в контроле за ВЭБ-инфекцией [6].…”